Evidence map›Paper›PMID 36459717›Full record

ArticleRedox biology2022

Myristoyl lysophosphatidylcholine is a biomarker and potential therapeutic target for community-acquired pneumonia.

Wengang Nan, Fen Xiong, Hong Zheng, Chen Li, Cong Lou, Xiong Lei, Huizhen Wu, Hongchang Gao, Yuping Li

Abstract read
In one paragraph

Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

  1. Trial
  2. The Polyphenol-EnrichedFoods (Basel, Switzerland) · 2026
    Article
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  5. Observational
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  7. Article
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  12. Observational
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Wengang NanDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Fen XiongOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Hong ZhengOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Chen LiOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Cong LouOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Xiong LeiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Huizhen WuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Hongchang GaoOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China. Electronic address: gaohc27@wmu.edu.cn.
Yuping LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. Electronic address: wzliyp@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is no gold standard for evaluating the severity of community-acquired pneumonia (CAP), and it is still based on a score. This study aimed to use the metabolomics method to find promised biomarkers in assessing disease severity and potential therapeutic targets for CAP. The result found that the metabolites in the plasma samples of CAP patients had significantly different between the acute phase and the remission phase, especially lysophosphatidylcholine (LPCs) in glycerophospholipids, whose levels are negatively linked to the severity of the disease. Subsequently, the two key metabolites of myristoyl lysophosphatidylcholine (LPC 14:0) and LPC 16:1 were screened. We analyzed the predictive performance of the two metabolites using Spearman-related analysis and ROC curves, and LPC14:0 showed more satisfactory diagnostic performance than LPC16:1. Then we explored the protective role and mechanism of LPC 14:0 in animal and cell models. The results showed that LPC 14:0 could inhibit the LPS-induced secretion of IL-1β, IL-6, and TNF-α, lower the ROS and MDA levels, and decreased the depletion of SOD and GSH, thereby reducing lung tissue and cell damage, such as down-regulating the protein level in BALF, lung W/D ratio, MPO activity, and apoptosis. We found that LPC 14:0 inhibited LPS-induced inflammatory response and oxidative stress, and the above protection was achieved by inhibiting LPS-induced activation of the NLRP3 inflammasome. LPC 14:0 may serve as a novel biomarker for predicting the severity of CAP. In addition, our exploration of the role of LPC 14:0 in animal and cellular models has reinforced its promise as a therapeutic target to improve the clinical efficacy for CAP.

Indexed as

LysophosphatidylcholinesPneumoniaAnimalsBiomarkersInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinBiomarkersInflammasomesLipopolysaccharidesLysophosphatidylcholinesNLR Family, Pyrin Domain-Containing 3 ProteinAcute lung injuryBiomarkerCommunity-acquired pneumoniaMetabolomicsNLRP3 inflammasome

Identifiers

PMID36459717
PMCPMC9712772

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.